Phacoemulsification-induced injury in corneal endothelial cells mediated by apoptosis: In vitro model

Geffen, Noa; Topaz, Moris; Kredy–Farhan, L.; Barequet, Irina S.; Farzam, Nahid; Assia, Ehud I.; Savion, Naphtali

doi:10.1016/j.jcrs.2008.08.024

Cited by 18 publications

(16 citation statements)

References 23 publications

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“…The changes in higher-order aberrations and total aberrations in diabetic patients are closely related to their age. Some studies have also shown that higher-order aberrations and total aberrations increase with age in patients with insulin-dependent diabetes mellitus [22] ( Table 5). In this study, higherorder aberrations also increased with age, but because the subjects in this study were children, their age range was small, which may explain the absence of statistical difference in this study.…”

Section: Discussionmentioning

confidence: 94%

Wavefront Aberration Analysis in Diabetic Children and Adolescents with Normal Vision

Wang¹,

Jia²,

T³

et al. 2020

Preprint

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Background: To compare the differences in wavefront aberrations between healthy and diabetic children with normal central vision and to investigate the causes of declined visual quality in diabetic children.Methods: This was a case-control study. Children with or without diabetes with normal central vision were selected as case and control group. The wavefront aberration parameters, including spherical aberration, coma aberration, root mean square of total wavefront aberration, root mean square of higher-order wavefront aberration, and corneal curvature, were measured by an automatic multifunctional ophthalmoscope. Statistical analysis was performed to determine the differences in average binocular wavefront aberration between groups. The correlations between wavefront aberration and age, visual acuity, corneal endothelium, intraocular pressure, axial length, corneal diameter, central corneal thickness, crystal thickness, anterior and posterior surface curvatures, and anterior chamber depth were analyzed in the diabetic group.Results: 32 patients with diabetes and 38 age- and sex-matched individuals were enrolled. The mean total and higher-order aberrations in diabetic group were slightly higher than those in control group, with no significant difference between groups (P > .05). The root mean squares of the aberrations correlated with anterior and posterior surface curvatures (P3mm = .014, P5mm = .021; P3mm = .035, P5mm = .038, respectively), but not with age, visual acuity, corneal endothelium, intraocular pressure, axis, corneal diameter, central corneal thickness, crystal thickness, and anterior chamber depth.Conclusions: For diabetic children, subtle changes in lens may lead to changes in wavefront aberrations and this may be the causes of visual impairment. These findings indicate the need to strengthen early screening and close follow-up of wavefront aberrations in diabetic children.Trial registration: This was a case-control study based on a hospital population (NCT 03587948). Date of registration was 07/03/2018. The name of the registration is Shanghai Children and Adolescent Diabetes Eye Study.

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Section: Discussionmentioning

confidence: 94%

Wavefront Aberration Analysis in Diabetic Children and Adolescents with Normal Vision

Wang¹,

Jia²,

T³

et al. 2020

Preprint

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“…It is known that apoptosis increases in the endothelium in PBK [11,12]. Apoptosis is an active process of programmed cell death which occurs with minimal damage to the surrounding cells [13].…”

Section: Discussionmentioning

confidence: 99%

Complement Activation in the Aqueous Humor of Pseudophakic Bullous Keratopathy Patients

et al. 2012

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Background/Aims: According to some studies, inflammation is a potential etiological factor in pseudophakic bullous keratopathy (PBK). Our aim was to obtain information on the activation of the complement system in the aqueous humor in this disorder. Methods: Aqueous humor samples were collected during keratoplasty of 12 PBK patients, as well as during phacoemulsification surgery of 18 control patients. The concentrations of the protein-protein complexes generated during complement activation (C1rC1sC1inh and C3bBbP) through the classical and alternative pathways, respectively, as well as of the C3 cleavage product C3a, were measured with ELISA methods. The correlation among the complement factors and between the duration of the edema, the stage of the disease, and the level of the complement activation products was examined. Results: The concentration of C1rC1sC1inh, C3bBbP complex and C3a was significantly higher in the PBK group (p < 0.001) compared to the control group. In PBK patients, a correlation was found between the levels of the C1rC1sC1inh complex and C3a only. Conclusion: Our new findings indicate that in PBK the complement system is activated – via the classical pathway – in the aqueous humor. The activated complement may play a role in increased endothelial cell loss.

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“…Any physical or pharmacological insult to this sensitive monolayer, therefore, implies the potential risk of corneal decompensation [25] . Many studies have shown that apoptosis is involved in this cell loss process [26][27][28] .…”

Section: Effects Of Bevacizumab Onmentioning

confidence: 99%

Effects of Bevacizumab on Apoptosis, Na<sup>+</sup>-K<sup>+</sup>-Adenosine Triphosphatase and Zonula Occludens 1 Expression on Cultured Corneal Endothelial Cells

et al. 2010

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Background: This laboratory study was undertaken to investigate the influence of bevacizumab on apoptosis, Na⁺-K⁺-adenosine triphosphatase (Na⁺-K⁺-ATPase) and zonula occludens 1 (ZO-1) expression on cultured human corneal endothelial cells (HCECs). Methods: Annexin V binding combined with propidium iodide (PI) costaining was used to distinguish viable, early and late apoptotic cells. Immunolocalization of ZO-1 and Na⁺-K⁺-ATPase was performed to analyze intercellular cell integrity after exposure to 5.0 mg/ml bevacizumab for 24 h. Results: No significant induction of apoptosis or necrosis was seen in HCECs after exposure to 5.0 mg/ml bevacizumab (p = 0.689, p = 0.516, respectively). The mean number of annexin-V-FITC- and PI-positive cells did not change significantly. Additionally, no significant changes in expression were detectable, neither for ZO-1 nor for Na⁺-K⁺-ATPase in comparison with the control. For ZO-1, 70.0% of the cells stained intensely, 24.7% stained moderately, and 5.3% stained weakly in the control group. After exposure to 5.0 mg bevacizumab, only minor changes were observable: 68.8% stained intensely, 25.4% moderately and 5.8% weakly (p = 0.524). For Na⁺-K⁺-ATPase, 19.3% of the cells stained intensely, 59.4% moderately, and 21.3% weakly in the control group. After exposure to 5.0 mg bevacizumab, again only minor changes were observable in the expression pattern: 18.2% stained intensely, 60.3% moderately and 21.5% weakly. The changes were not significant compared with the control (p = 0.492). Conclusions: Bevacizumab, at concentrations used clinically, did not induce apoptosis or necrosis in HCECs in vitro. Additionally, no alteration of ZO-1 or Na⁺/K⁺-ATPase expression was detected after exposure to 5.0 mg/ml bevacizumab for 24 h.

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Phacoemulsification-induced injury in corneal endothelial cells mediated by apoptosis: In vitro model

Cited by 18 publications

References 23 publications

Wavefront Aberration Analysis in Diabetic Children and Adolescents with Normal Vision

Wavefront Aberration Analysis in Diabetic Children and Adolescents with Normal Vision

Complement Activation in the Aqueous Humor of Pseudophakic Bullous Keratopathy Patients

Effects of Bevacizumab on Apoptosis, Na<sup>+</sup>-K<sup>+</sup>-Adenosine Triphosphatase and Zonula Occludens 1 Expression on Cultured Corneal Endothelial Cells

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